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ECG EXAMINATION Seminary of pathophysiology Pavel Maruna

ECG EXAMINATION Seminary of pathophysiology Pavel Maruna. Electrical conduction in heart. SA node (= pacemaker). AV node. Bundle of His. Right and left bundle branches. Purkynje fibres. Cellular depolarization . What do we measure? What is positive and negative vector?.

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ECG EXAMINATION Seminary of pathophysiology Pavel Maruna

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  1. ECG EXAMINATION Seminary of pathophysiology Pavel Maruna

  2. Electrical conduction in heart SA node (= pacemaker) AV node Bundle of His Right and left bundle branches Purkynje fibres

  3. Cellular depolarization • What do we measure? • What is positive and negative vector?

  4. 12-lead ECG examination Limb leads aVL aVR Bipolar leads I, II, III Pseudounipolar leads aVR, aVL, aVF aVF

  5. 12-lead ECG examination Chest leads Unipolar leads

  6. 12-lead ECG examination

  7. QRS axis (Axis of QRS complex depolarization) - 30° to + 105°

  8. initiation of impulse in the SA node

  9. initiation of impulse in the SA node atrial depolarization

  10. initiation of impulse in the SA node atrial depolarization depolarization of AV nodus and bundle of His

  11. septal depolarization

  12. septal depolarization early ventricular depolarization

  13. septal depolarization early ventricular depolarization late ventricular depolarization

  14. ventricular systole

  15. ventricular systole ventricular repolarization

  16. ventricular systole ventricular repolarization repolarization of bundle of His

  17. PR (PQ) interval (0,12 - 0,20 s) QTc interval (to 0,44 s) QRS complex (0,06 - 0,10 s)

  18. What to see on the curve? • Rhythm? • P wave • Intervals • QRS complex • ST segment • T wave (U wave)

  19. P wave Electrical impulse originates in the SA node Impulse triggers atrial depolarization • Physiology: • positive orientation (possible biphasic in I lead) • duration < 0,11 s, amplitude < 2,5 mm • Pathology: • hypertrophy of left or right atrium • abnormal conduction (SVES)

  20. P wave P mitrale High P amplitude due to left atrial hypertrophy

  21. PR (PQ) interval depolarization of AV node and bundle of His It represents the physiological delay in conduction from atrial depolarization to the beginning of ventricular depolarization. It is electrically neutral. Limits: 0,12 - 0,20 s Physiological importance: 1. synchronization of both atrial and ventric. systoles 2. protection against the transmission of supraventricular tachyarrhythmia to vetricular tachycardia

  22. PR (PQ) interval AV blockade 1st = prolongation of PR interval 2nd = partial blockade (transmission of selected impulses) - Wenckenbach - Mobitz

  23. PR (PQ) interval AV blockade 3rd = complete blockade

  24. QRS complex Depolarization of the ventricles • Physiology: • duration 0,06 - 0,10 s • Q < 0,04 s, < 25 % of R wave • Sokolow index (S in V2 + R in V5) < 35 mm (< 45 mm for young) • axis of ventricular depolarization -30 to +105 °

  25. QRS complex • Physiology: • duration 0,06 - 0,10 s • Q < 0,04 s, < 25 % of R wave • Sokolow index (SV2 + RV5) < 35 mm (< 45 mm for young) • axis of ventricular depolarization -30 to +105 ° • VAT (ventricular activation time) of LV < 0,04 s, RV < 0,03 s

  26. QRS complex Both QRS complex duration and shape is depend on: 1. Physiology of His-Purkine´s system or aberrant signal passing VES

  27. QRS complex Both QRS complex duration and shape is depend on: 1. Physiology of His-Purkine´s system or aberrant signal passing RBBB ...................... (QRS prolongation, rSR´ in V1, negative T wave) Intraventricular blockades V1

  28. RBBB

  29. QRS complex Both QRS complex duration and shape depend on: 2. Myocardial mass LV hypertrophy RV hypertrophy cardiomyopathy

  30. QRS complex wide QRS complex Both QRS complex duration and shape is depend on: 3. Factors affecting signal velocity - metabolic, endocrine, and pharmacological high sharp T wave hyperkalemia

  31. QRS complex Both QRS complex duration and shape is depend on: 3. Factors affecting signal velocity - metabolic, endocrine, and pharmacological digitalis

  32. QRS complex Prolongation Shortening LV, RV hypertrophy diffuse alteration (amyloid, fibrosis) hyperkalemia, digoxin artificial factors (obesity, pericard. effusion) intraventricular blockade VES

  33. QRS complex Pathological Q wave Q wave prolongation (> 0,04 s) and depression (> 25 % R) Manifestation of transmural myocardial necrosis „Cavity potential“

  34. Patological Q

  35. ST segment The length between the end of the S wave (end of ventricular depolarization) and the beginning of repolarization • From „J point“ on the end of QRS complex, to inclination of T wave • Normally, all cells have the same potential = ST segment is electrically neutral (on isolectric line)

  36. ST segment Physiological changes sympathicus ... ST depression, „anchor-like“ curve parasympathicus (vagus) ... ST elevation syndrome of an early repolarization Artificial changes depend on lead localization, chest malformation etc. Patological changes electric potential of destroyed myocardial area

  37. ST segment Ischemic focus has a different electric potential = electric vector leads to this area 1. subendocardial ischemia (non-Q MI, AP paroxysm) ... ST depresssion

  38. ST segment Ischemic focus has a different electric potential = electric vector leads to this area 2. subepicardial ischemia (Q-MI, spastic form of AP, aneurysma) ... elevation of ST segment

  39. T wave Ventricular repolarization Normally: a repolarization directs from epicardium to endocardium = T wave is concordant with QRS complex Ischemic area: a repolarization is delayed, an action potential is extended Vector of repolarization is directed from ischemic area: - subendocardial ischemia ... to epicardium ... T wave elevation - subepicardial ischemia ... to endocardium ... T wave inversion

  40. T wave • LV overload • neurocirculatory asthenia • sympathetic system • hypokalemie • hyperglycemia • myxoedema • pancreatitis • pneumotorax Nonspecific changes Diffuse T changes, T wave asymmetric or biphasic

  41. T wave Ischemia Nonspecific changes Localized T changes T wave - symmetric negativity Diffuse T changes, T wave asymmetric or biphasic

  42. K+ influence on cardiac conductivity

  43. Refractory period 1. Absolute = Absolutely no stimulation can cause another action potential 2. Relative = It is possible to cause another action potential, but the intensity of the premature contraction will be relative to the time in this period. „R on T“ phenomena „Malignant VES“: R wave of the next beat falls in certain portions of the previous T-wave ... Serious and life-threatening arrhythmia

  44. Holter monitoring 24-h ECG recording Ambulatory ECG device Analysis of mean, maximal, and minimal HR, occurrence and frequency of major arrhythmia Confrontation of record and subjective difficulties (patient activity log) Indications: 1. syncope or palpitation of unclear origin 2. an unveiling of latent ischemia 3. an antiarrythmic therapy control 4. a pacemaker control

  45. Holter monitoring Patient No. 1 Finding of atrial fibrillation. Pauses > 2 s Rare ventricular ES

  46. Holter monitoring Patient No. 2 Ventricular fibrillation

  47. Holter monitoring Patient No. 3 Ventricular tachycardia

  48. Ergometry, exercise ECG Gradual load increase in 4-min. intervals, basic level 25 - 75 W Stopping - submaximal load or complications (accelerated hypertension, polytopic VES, blockades, ST elevation ST, ST depression > 2 mm, T inversion Coincidence of chest pain + ST changes = confirmation of ischemia Indications: 1. specification of ischem. disease prognosis 2. suspicion on ischemic disease 3. examination of functional capacity

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